Research on the effects of acute alcohol intoxication on negative affect has been dominated by the Stress Response Dampening perspective, which suggests that alcohol reduces negative affective response to aversive stimuli through direct pharmacological suppression of activity in the primary subcortical fear system. However, recent compelling demonstrations of differential effects of alcohol on fear response dependent upon the cognitive processing requirements of the fear-eliciting cue suggest a more complex mechanism. Current advances in animal models of the neural circuitry of fear indicate that fear cues are processed through multiple, parallel pathways from subcortical and cortical structures into the primary subcortical fear system, with different pathways responsible for processing different characteristics of the cues. Synthesis of these neuroscience findings with the recent observed dissociations in alcohol's effect on fear suggests that alcohol does not directly affect the primary subcortical defensive system but instead exerts its influence on fear through its deleterious effects on specific cortical structures and pathways required for cognitive appraisal of certain emotionally evocative stimuli. The current project will examine human fear conditioning in intoxicated and non-intoxicated individuals, indexed with fear potentiated startle (FPS), in two distinct cuing conditions. These conditions will involve either 1) Cues which require higher-order cognitive processing (e.g., memory for context) that is mediated by the hippocampus and affiliated brain structures (i.e., contextual fear conditioning); or 2) Simpler, explicit cues not requiring such complex processing (i.e., explicit-cue fear conditioning). Substantial neuroscience research exists to indicate that different neural pathways and cognitive systems/structures are required for the development of conditioned fear to these two different sets of cues. Therefore, dissociation in alcohol's effect on fear across these cuing conditions would indicate that this drug's effect on emotion is mediated by specific higher brain processes and pathways, rather than produced by the direct action on the primary fear system. In line with the hypothesis that alcohol affects emotional responsivity indirectly, through its impact on higher Drain regions including the hippocampus, the primary aim of this experiment is to determine whether ethanol ingestion selectively impairs acquisition and/or expression of contextual conditioning, but leaves explicit-cue conditioning intact in humans.